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Four main etiologic factors have been implicated in the pathophysiology of acne: sebaceous gland hyperactivity, inflammation, abundance of Propionibacterium acnes, and dysfunction of the desquamation of the hair follicle (see Chapter 64, Anti-inflammatory Agents). These causal elements work interdependently and are mediated by such important influences as diet, stress, heredity, and hormonal activity.
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SEBACEOUS GLAND HYPERACTIVITY
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Sebum, composed of lipids, is continuously synthesized by the sebaceous glands and secreted to the skin surface through the hair follicle pore. The sebaceous glands are located all over the body but are largest and most numerous in the face, back, chest, and shoulders. These glands become more active during puberty because of the increase in androgens, particularly testosterone, which spurs sebum production. Oral drugs that inhibit sebaceous gland activity, such as antiandrogens, estrogens, and retinoids, are important treatment modalities in the successful control of acne. At this time, there are no topical ingredients that can reduce sebum secretion, most likely because the sebaceous gland is deep in the hair follicle and unreachable by most topical agents.
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FOLLICULAR KERATINIZATION
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The keratinocytes that line the hair follicle undergo the maturation process known as keratinization. Once they mature into stratum corneum cells, they desquamate into the hair follicle. In acne patients, these keratinocytes have a tendency to stick together due to the effects of positive and negative charges, the actions of the enzyme transglutaminase, and the viscosity of sebum. The clumped keratinocytes block the pore/follicle, creating a blackhead if the pore is open (“open comedone”) or a whitehead if it is closed (“closed comedone”). The clogged pore is a great nutritional source for P. acnes bacteria.
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THE INFLUENCE OF BACTERIA
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P. acnes has been cited as a key component in the etiologic pathway of acne, a sine qua non feature, because it is typically present in higher concentrations in teenagers with acne than in controls without acne.1 When P. acnes is present, immune system cells are activated to initiate an inflammatory immune response. In addition, P. acnes itself releases inflammatory mediators when it ingests sebum. This inflammation leads to the red pus-filled bump known as a “pimple.”
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Corynebacterium acnes is another bacteria associated with the pathophysiologic pathway of acne. Antibiotic resistance to P. acnes bacteria is estimated to be as high as 60 percent in some patient populations.2 Erythromycin, methicillin, and clindamycin are the most common antibiotics to which bacteria have been reportedly found to be resistant.3 For this reason, erythromycin and clindamycin should no longer be used as monotherapy for acne. Benzoyl peroxide (BPO), lauric acid, triclosan, and colloidal silver display antibacterial properties that make them attractive as antiacne agents that should not lead to bacterial resistance.4–6 Combining BPO with erythromycin or clindamycin has been proven to prevent the emergence of resistant strains ...